RESUMEN

The aim of this study is to evaluate the role of serum level of Interleukin 6(IL-6) and Interleukin 17 (IL-17) in liver transplantation outcome for living recipients, Analyze the relation between the gene polymorphism and the occurrence of rejection after liver transplantation and Study the relation between the gene polymorphism and the occurrence of different infectious complications. The study was conducted in March 2023 and included 60 healthy volunteers from the National Liver Institute (NLI) blood bank at Menoufia University and 120 live donation liver recipient patients at NLI. During one month of liver transplantation, the cytokine levels (IL-17, IL-6 proteins, IL-6 G-174C, and IL-17 A rs2275913 gene polymorphism) and CD4 levels for 60 patients of 120 live donation liver recipient patients whom early reject transplanted tissue and the same parameters were measured after 6 months follow up for non-reject group. The main finding of this study was that the post-transplant rejection group and the post-transplant non-rejection and control groups differed significantly in the genotype frequency (CC, CG, and GG) or alleles of IL-6 G-174C (p = 0.011). On the other hand IL-17A rs2275913 gene polymorphism and its alleles (p = 0.71) showed no statistically significant difference. We also observed that serum IL-17 levels, with 100% specificity and 100% sensitivity threshold, will be more sensitive and specific than serum IL-6 and CD4 count in differentiating post-transplant rejection from non-rejection patients. The results showed that there was no significant relationship between the genotypes and serum levels of interleukins and the type and degree of rejection. Proinflammatory cytokines might be useful indicators for distinguishing and early identifying unfavorable outcomes after transplantation, allowing for prompt and effective treatment intervention. To evaluate these findings, prospective clinical trials are required.

Asunto(s)

Rechazo de Injerto , Interleucina-17 , Interleucina-6 , Trasplante de Hígado , Donadores Vivos , Polimorfismo de Nucleótido Simple , Humanos , Trasplante de Hígado/efectos adversos , Interleucina-17/sangre , Interleucina-17/genética , Rechazo de Injerto/genética , Rechazo de Injerto/sangre , Masculino , Femenino , Persona de Mediana Edad , Interleucina-6/sangre , Interleucina-6/genética , Adulto , Genotipo , Aloinjertos , Alelos , Receptores de Trasplantes

RESUMEN

The goal of this study is to investigate the impact of the rs35829419 SNP on the serum level of NLRP3, and to assess the relationship between NLRP3 and its SNP and vulnerability to Pityriasis versicolor. Pityriasis versicolor (PV) is one of the most frequent skin conditions linked to skin pigmentation changes. Malassezia plays a key role in the pathogenesis of PV. A case-control study, 50 patients with pityriasis versicolor and 44 healthy controls. Real-time PCR was used to genotype NLRP3 (rs35829419) and ELISA assay of NLRP3 levels in tissue samples. There was a significantly higher median NLPR3 levels in PV patients than controls. A significant predominance of A allele of Q 705 K was in patients than controls. The risk of having the disease in the presence of A allele is nearly 10 times than having C allele. In PV patients, there was a significant relationship between NLPR3 levels and Q 705 K genotypes with higher NLPR3 levels in AA genotype. A potential correlation between PV and the Q705K polymorphism, pointing to evidence of NLRP3 alteration in PV patients. The NLRP3 inflammasome may be an appropriate therapeutic target for Malassezia-associated skin disorders.

Asunto(s)

Genotipo , Inflamasomas , Proteína con Dominio Pirina 3 de la Familia NLR , Polimorfismo de Nucleótido Simple , Piel , Tiña Versicolor , Humanos , Tiña Versicolor/diagnóstico , Tiña Versicolor/genética , Tiña Versicolor/microbiología , Proteína con Dominio Pirina 3 de la Familia NLR/genética , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Femenino , Masculino , Estudios de Casos y Controles , Adulto , Inflamasomas/genética , Inflamasomas/metabolismo , Inflamasomas/inmunología , Piel/patología , Piel/microbiología , Malassezia/aislamiento & purificación , Malassezia/inmunología , Malassezia/genética , Adulto Joven , Predisposición Genética a la Enfermedad , Persona de Mediana Edad , Alelos , Adolescente

RESUMEN

OBJECTIVES: This study aims to examine whether the genetic variants in the genes for Granzyme B (GZMB) and Interferon Induced with Helicase C domain 1 (IFIH1) were associated with psoriasis. BACKGROUND: Psoriasis, a papulosquamous skin disease, was initially thought of as a disorder primarily of epidermal keratinocytes but is now recognized as one of the most common immune-mediated disorders. It is caused by the interplay between multiple genetic and environmental risk factors. SUBJECTS AND METHODS: This case-control study has 65 participants with psoriasis and 65 healthy controls. Real-time PCR was used to genotype GZMB (rs8192917) and IFIH1 (rs35667974). RESULTS: Genotype occurrence and allelic spreading for both SNPs are in Hardy - Weinberg equilibrium. The genotype and allele distributions of rs35667974 showed no differences between the studied groups. Regarding rs8192917, compared to Group II, there is a statistically significant rise in the CC genotype and C allele in Group I. Higher PASI scores are detected in the C/C and C/T genotypes more than the T/T genotype. Univariate and multivariate analyses revealed that BMI, catalase, MDA, and rs8192917 (C/C) are associated with psoriasis. CONCLUSION: GZMB rs8192917 was significantly related to psoriasis risk; its C allele is likewise associated with psoriasis vulnerability. However, our investigation found no link between rs35667974 and psoriasis.

Asunto(s)

Granzimas , Helicasa Inducida por Interferón IFIH1 , Psoriasis , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Adulto Joven , Estudios de Casos y Controles , Egipto , Predisposición Genética a la Enfermedad , Genotipo , Granzimas/genética , Helicasa Inducida por Interferón IFIH1/genética , Helicasa Inducida por Interferón IFIH1/inmunología , Pueblo Norteafricano , Polimorfismo de Nucleótido Simple , Psoriasis/genética

RESUMEN

BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune disease that influences numerous body systems. Furin, tristetraprolin (TTP), and NOD, LRR, and pyrin domain-containing protein 3 (NLRP3) contribute in developing autoimmune illnesses. AIM: Understandthe role of furin, TTP, and NLRP3 mRNA gene expression in SLE pathogenesis and prognosis. Methods: Total 210 individuals were enrolled, divided in two group: cases and control; 105 participants in each group.  Real-time quantitative PCR for furin, TTP,and NLRP3 mRNA gene expression were determined for each subject. RESULTS: SLE patients showed significantly higher serum furin [median 20.10 (0.0-162.88) in comparison with control group [median 1.10 (0.33-8.64)] with significant pvalue (p < 0.001), for NLRP3 expression [median 7.03 (0.0-282.97) compared to control group [median 1.0 (0.44-9.48)] with significant p value (p = 0.006)but lower TTP [median 2.37 (0.0-30.13)] in comparison with control group [median 7.90 (1.0-29.29)] with significant p value (p < 0.001) . Elevated levels of Furin and NLRP3 and low levels of TTP were linked to increased illness activity. CONCLUSION: Furin and NLRP increase in SLE and higher with illness activity. TTP is lowerin SLE and negatively correlates with disease activity.

Asunto(s)

Lupus Eritematoso Sistémico , Proteína con Dominio Pirina 3 de la Familia NLR , Humanos , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Furina , ARN Mensajero/genética , ARN Mensajero/metabolismo , Lupus Eritematoso Sistémico/diagnóstico , Lupus Eritematoso Sistémico/genética , Biomarcadores

RESUMEN

BACKGROUND: Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and the leading cause of cancer mortality. Various studies have linked dysregulated microRNA expression to liver cancers, but those related to viral hepatitis-related HCC are limited. METHODS: We investigated the diagnostic and prognostic roles of circulating miR-331-3p, miR-23b-3p, and miR-3194-5p in EDTA-treated blood samples of 50 hepatitis C virus (HCV) HCC patients, 50 HCV cirrhotic patients, and 50 healthy controls using quantitative real-time polymerase chain reaction. RESULTS: We found that miR-23b-3p and miR-3194-5p were significantly downregulated, whereas miR-331-3p was upregulated in HCC patients compared with controls. Also, these miRNAs were significantly dysregulated in HCC compared with cirrhotic patients. For the diagnosis of HCC, miR-331-3p and the combined miRNAs panel had the highest area under the curve (AUC), followed by miR-3194-5p. The highest AUC for differentiating metastatic from nonmetastatic patients was shown by miR-331-3p and the combined miRNAs panel, followed by miR-23b-3p. Dysregulation of miRNAs was associated with poor clinicopathological manifestations. Finally, miR-331-3P was found to be an independent risk factor for metastatic lesions in HCC. CONCLUSION: Overall, the assessed miR-331-3p, miR-23b-3p, and miR-3194-5p were significantly associated with poor clinicopathological features of HCC and could be used to discriminate HCV-related HCC patients from cirrhosis and differentiating metastatic from nonmetastatic patients, primarily miR-331-3p along with combined miRNAs. Moreover, miR-331-3p was found to be an independent factor for metastatic lesions.